02449nas a2200373   4500000000100000008004100001260001300042653003800055653002700093653001000120653001400130653003800144653002000182653002600202653003000228653001700258653001100275653001100286653001200297653002800309653001400337653000900351653001600360100001500376700001300391700001200404700001200416245019200428856010100620300001100721490000700732520132200739022001402061       2007                            d  c2007 Oct10aAcetylmuramyl-Alanyl-Isoglutamine10aAdjuvants, Immunologic10aAdult10aApoptosis10aBacterial Outer Membrane Proteins10aCells, Cultured10aDrug Delivery Systems10aEscherichia coli Proteins10afas Receptor10aFemale10aHumans10aleprosy10aLeukocytes, Mononuclear10aLiposomes10aMale10aMiddle Aged1 aChattree V1 aKhanna N1 aBisht V1 aRao D N00aLiposomal delivery of Mycobacterium leprae antigen(s) with murabutide and Trat peptide inhibits Fas-mediated apoptosis of peripheral blood mononuclear cells derived from leprosy patients.  uhttp://nopr.niscair.res.in/bitstream/123456789/140/1/IJBB%2044%285%29%20%282007%29%20386-393.pdf  a386-930 v443 a<p>Protective immunity against intracellular pathogen Mycobacterium leprae is dependent on the activation of T cells. Repeated stimulation of T cells by M. leprae antigens MLCwA (M. leprae total cell wall antigen) and ManLAM (mannose capped lipoarabinomannan) may lead to apoptosis in leprosy patients. In the present study, inhibition of the Fas-induced apoptosis of peripheral blood mononuclear cells of leprosy patients was investigated using above M. leprae antigen(s), in combination with immunomodulators murabutide (MB) and a Trat peptide in particulate form (liposome). Incubation of the cells with particulate mode of antigen presentation led to both decreased percentage of propidium iodide (PI) positive cells and T cells expressing Fas-FasL, as well as decreased caspase-8/-3 activities in the lepromatous patients, thereby inhibiting apoptosis, while converse was true with stimulation with soluble antigen. Concurrently, there was an upregulation of antiapoptotic protein Bcl-X(L) in the lepromatous patients, thereby inhibiting apoptosis. Thus, the liposomal formulation of antigen promoted proliferation of anergized T cell by inhibiting apoptosis through decreased expression of death receptors and caspase activities and increased expression of anti-apoptotic protein Bcl-X(L) in these patients.</p>  a0301-1208